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PubMed1981

Report on international comparative evaluation of possible value of assays for immune complexes for diagnosis of human breast cancer.

There have been several reports on the possible value of measurements of circulating immune complexes for the diagnosis of human breast cancer. To begin to evaluate this possibility and the comparability of results among laboratories, a cooperative study was organized under the auspices of the International Agency for Research on Cancer and the National Cancer Institute (NCI) of the United States. Investigators from four laboratories performing assays for immune complexes were sent coded aliquots of serum specimens from the NCI-Mayo Clinic Serum Bank. The serum panel consisted of specimens from 30 patients with breast cancer (including 20 from untreated patients with resectable tumors), 30 preoperative patients with benign breast disease, and 30 normal women. Although some significant differences in levels of immune complexes between cancer patients and controls were seen, none of the assays had sufficient discriminatory capacity to support optimism about the diagnostic value of this approach. To relate the results with immune complexes to those with a widely used cancer marker, the same sera were also tested for levels of carcinoembryonic antigen (CEA). The CEA assay provided significant discrimination between cancer patients and normal donors but did not significantly discriminate between malignant and benign breast diseases.

Antigen-Antibody Complex↗
PubMed1984

A comparison of the properties of two classes, C4A and C4B, of the human complement component C4.

A remarkable difference has been observed between the reactivity of the two forms of human complement component C4. C4B binds twice as effectively as C4A to antibody-coated red cells, but the reverse occurs with protein-antigen complexes. C4B reacts much more effectively with hydroxyl groups than C4A and this is reversed for reaction with amino groups in spite of the very small difference in amino acid sequence between the two forms of C4. No other differences in stability, activation or inactivation were observed. These findings emphasise the biological advantage of the duplication of the C4 gene in its reaction with a wide range of antigenic structures. The correlation of the presence of different forms of C4 with susceptibility to autoimmune diseases may be explicable by these big differences in binding reactivity.

Amino Acid Sequence↗
PubMed1994

Synthetic polysulfated hyaluronic acid is a potent inhibitor for tumor necrosis factor production.

Based on the premise that naturally occurring glycosaminoglycans could serve as building blocks for synthesizing nontoxic drugs for suppression of tumor necrosis factor (TNF) production by inflammatory cells, we have chemically modified hyaluronic acid (HA) and tested its effects in blocking TNF-alpha and TNF-beta production in vitro. HA was chosen mainly for its structural simplicity, nonimmunogenicity, and readiness for chemical modifications. When HA was chemically polysulfated to a sulfate/hexosamine molar ratio of 3.9, the sulfated HAs was shown to be a potent inhibitor of TNF-alpha production in lipopolysaccharide (LPS)- or interferon-gamma-activated THP-1 cells. For example, a concentration of HAs as low as 10 ng/ml reduced TNF-alpha production in LPS-activated THP-1 cells more than 50%, whereas achieving a similar extent of reduction required 50 micrograms/ml native HA. By decreasing the extent of polysulfation, the inhibitory effect of HAs on TNF-alpha production was diminished. Other chemical modifications, including deacetylation, thiolation, or reduction of the carboxylic groups, could not increase the efficacy of HA in suppression of TNF-alpha production. Naturally polysulfated glycosaminoglycans, such as chondroitin sulfates, keratan sulfate, heparan sulfate, and heparin, failed to inhibit TNF-alpha production. HAs also restricted TNF-beta (lymphotoxin) secretion in an Epstein-Barr virus-transformed B cell line, Roha-9, which constitutively produces TNF-beta. HAs had no inhibitory effect on the proliferation of THP-1 or Roha-9 cells, which would account for the reduced TNF-alpha or TNF-beta production. Furthermore, time-course metabolic labeling studies revealed that HAs could not restrict overall protein synthesis and secretion in THP-1 cells. However, HAs increased complement C1q secretion in THP-1 in a dose-dependent manner, but it had no effect on biosynthesis of complement C1 inhibitor, factor D, and Fc gamma receptor type II (Fc gamma RII). These results indicate that HA, selectively restricts the production of TNF-alpha, TNF-beta, and probably several other protein species.

Cell Division↗
PubMed1981

Hemolytic complement and its components in Syrian hamsters: a study of five strains uninfected and infected with Brugia pahangi.

Complement profiles were tested in outbred (LVG) Syrian hamsters (Mesocricetus auratus) and compared to the MHA, LHC, PD4, and CB inbred strains. The total C and C component concentrations in the sera varied among the strains and were in the following ranges in untreated animals (in CH50 units per ml): total C, 140-260 (undetectable in PD4 and CB); Cl, 14,000-25,000; C2, 200-800 (except PD 4 and CB); C3, 40,000 and 80,000; C4, 2,000-2,800 (except PD4 and CB); C4, 40,000-80,000; C6, 3,600-6,000 (undetectable in PD4 and CB); C7, 50,000-350,000; C8, 10,000-30,000; C9, 30,000-60,000. The PD4 and CB strains had undetectable total C and C6, and their exact C2 and C4 levels could not be determined, but were lower than in the other strains. The MHA strain had the highest total C levels, but had significantly lower (1/3 or less) C7 levels than the other strains of hamsters. Infection of hamsters with the filarid nematode Brugia pahangi for four to five months produced moderate decreases in the total C and C3 levels, but varied changes in other C components. Six infected and three uninfected animals died during the experiment from spontaneous enteritis and weight loss.

Animals↗
PubMed1995

Complement activation in amyloid plaques in Alzheimer's disease brains does not proceed further than C3.

In Alzheimer's disease (AD) patients, the complement components Clq, C4 and C3 can be detected in different types of beta/A4 plaques, one of the hallmarks of AD. Contradictory findings on the presence of late complement components in AD brains have been reported. Nevertheless, it was suggested in recent studies that in AD brain complement activation results in complement membrane attack complex (MAC) formation and that complement activation may act as an intermediate between beta/A4 deposits and the neurotoxicity observed in AD. In the present study the presence of a number of complement components and regulatory proteins in AD temporal cortex and, for comparison, in glomerulonephritis (GN) was analysed. In GN kidneys, besides Clq, Clr, Cls and C3, the late components and the C5b-9 complex are also associated with capillary basement membrane and mesangial immune complex deposits. In AD temporal cortex Clq, C4 and C3 are co-localized with beta/A4 deposits. However, in contrast to the GN kidney, the late complement components C5, C7 and C9, as well as the C5b-9 membrane attack complex cannot be detected in beta/A4 positive plaques. The absence of the cytolytic C5b-9 complex in AD brain suggests that in AD, the complement MAC does not function as the proposed inflammatory mediator between beta/A4 deposits and the neurofibrillary changes.

Aged↗
PubMed1988

C1q production and C1q-mediated immune complex retention in lymphoid follicles of rat spleen.

Involvement of C1q in retaining immune complexes in germinal centers in rat spleen was studied in vivo and in vitro. C1q production was found in fibroblastic reticulum cells in the peripheral mantle zone, in follicular dendritic cells in germinal centers, and in transitional forms between these two cells in the inner mantle zone. In passively immunized animals, immune complexes were found transiently on fibroblastic reticulum cells, then on the transitional forms and follicular dendritic cells. Extracellular C1q was detected by the presence of immune complexes on both the transitional forms and follicular dendritic cells, but not on fibroblastic reticulum cells. Thus, the fibroblastic reticulum cell appeared to trap immune complexes but not to retain either immune complexes or C1q. The morphology and function of the fibroblastic reticulum cell and the follicular dendritic cell suggest that they belong to the same lineage. Immune complexes were bound in vitro to germinal centers in cryostat spleen sections in the same manner as those retained in vivo. The binding required no complement in the incubation medium and was inhibited by C1q-suppressing factors. The extracellular C1q originating from the follicular cells may therefore play a role in retaining immune complexes in the germinal center.

Animals↗
PubMed1988

A homozygous point mutation results in a stop codon in the C1q B-chain of a C1q-deficient individual.

Southern blot analysis of the B-chain genes in one of eight C1q-deficient individuals revealed an abnormal banding pattern. The defect, which was homozygous, could be localized by restriction mapping to a single Taq I site within residue 150 in the coding region of the B-chain gene. DNA sequencing across the site revealed a stop codon that would cause premature termination of the protein product. No material corresponding to the A or C chains, or a truncated B chain, could be identified by antigenic analysis of the patient's serum, indicating that a complete B chain is required for secretion of a C1q molecule.

Codon↗
PubMed1978

Complement system activation by contrast media in neuroradiology.

Complement system activation was studied in six series of 12 patients undergoing routine contrast study following IV injection of five recently developed contrast media. The decreasing order of effectiveness on the complement system was as follows: ioxaglic acid, metrizamide, iodamidol. Metrizoic and ioxithalamic acids did not provoke any complement depletion at the doses used in this study. Both pathways of activating the complement system were involved. We could not find any definite correlation with osmolarity, ionic or nonionic formulation, protein binding, or hydrophobicity.

Complement Activation↗
PubMed1986

Inhibition of C1q binding to antigen-antibody complexes by a factor in rheumatoid arthritis serum.

The sera and synovial fluids of patients with rheumatoid arthritis (RA) contain a factor which decreases the binding of C1q to antigen-antibody complex (IC). Several lines of evidence suggest that this factor is distinct from the documented C1q inhibitor which is a chondroitin sulphate. It binds to IC rather than to C1q. It is resistant to digestion with chondroitinase ABC. The addition of chondroitin sulphate to serum does not inhibit the binding of IC to C1q. The observation that three purified IgM and IgG rheumatoid factors (RF) did not reduce C1q binding to IC indicates that the factor is not RF. The ability of RA sera to reduce IC binding to C1q was inversely correlated with their ability to prevent immune precipitation (PIP), and directly with levels of an inhibitor of PIP. These data suggest that the factor which binds to IC and reduces C1q binding may be responsible for the excessive immune precipitation which occurs in RA sera.

Antigen-Antibody Complex↗
PubMed1986

Anti-C1q affinity isolated circulating immune complexes correlate with extra-articular rheumatoid disease.

Circulating immune complexes (CIC) were isolated from sera of 35 patients with rheumatoid arthritis (RA) by a two-step method using 2% polyethylene glycol precipitation and anti-C1q affinity chromatography. By this method CIC were exclusive to 19 patients with vasculitis, nodules, or Sjögren's syndrome. Levels of CIC did not correlate with the severity of synovitis but reflected the extent of extra-articular disease. Furthermore, in four patients with persistent severe synovitis observed over a period of 4 to 16 months, the levels of CIC paralleled changes in extra-articular disease. Despite such additional evidence, whether the relationship between CIC and tissue injury is causative or consequential remains unresolved.

Aged↗
PubMed1975

[Pathomorphogenesis of blistering in epidermolysis bullosa acquisita and epidermolysis bullosa dystrophica (author's transl)].

Electronmicroscopical examination on skin lesions of epidermolysis bullosa dystrophica recessiva (E.b.d.r.) and epidermolysis bullosa acquisita (E.b.a.) associated with Crohn's disease have demonstrated that blistering occurs between epidermis and dermis beneath the basal lamina. The structural defect concerns the anchoring fibrils only which are missing in the junctional zone of the involved skin. All other junctional structures are intact. Beneath the basal lamina a band-like zone of a moderate electrondense, amorphous material is seen in the skin-lesions of epidermolysis bullosa acquisita, less marked in epidermolysis bullosa dystrophica. Direct immunofluorescent investigation of involved skin of E.b.a. shows a pemphigoid-like fluorescent pattern at the basal lamina with antihuman IgG-, -IgM-, beta1c/beta1a and antihuman C1q-component. In epidermolysis bullosa dystrophica, however, a fluorescent pattern at the basal lamina was found only with anti-human IgG and Anti-C3. The pathogenetic importance of the immunoglobuline-deposits at the basal lamina is discussed in regard of the loss of anchoring fibrils and the subsequent vesication in these types of epidermolytic diseases.

Animals↗